In order to answer the questions if and how various
factors can alter compensatory eye movements and how the cerebellum
contributes to these changes, we investigated the eye movements of a
laboratory mouse. By using an integrated and multidisciplinary
approach of genetic techniques, cellular physiology, and behavioral
experiments in various mouse models, we were able to tackle some of
these questions.
We can conclude that various factors influence cerebellar plasticity
and cerebellar motor learning and that measuring compensatory eye
movements is a powerful technique to investigate these factors.
Compensatory eye movements rely on a multisensory integration system
that induces execution of accurate eye movements in time and space.
This multisensory integration system has also the capacity to
compensate for certain deficits.
Adaptation of compensatory eye movements is mediated by the olivo -
cerebellar circuit that utilizes multiple mechanisms to recalibrate
its output. The processes that involve acquisition and storage of the
altered behavioural responses do not solely rely on long-term
depression (LTD) and long-term potentiation (LTP) at parallel fiber to
Purkinje cell synapse but also on LTP at mossy fiber to granule cell
synapse.
Estradiol induces morphological changes and electrophysiological
synaptic plasticity changes in the cerebellum that are well correlated
with the cerebellum-dependent behavioral output.